Search

Background: Coronary artery calcification (CAC) is commonly assessed with Agatston score (AS). A higher sensitivity and precision for the detection of CAC has been demonstrated with calibrated mass score (cMS). We hypothesized that cMS would detect low-level CAC not detectable with AS in a large asymptomatic background population.Methods: Participants (N = 2985) from the Copenhagen General Population Study were evaluated for CAC using both conventional AS and cMS. The population was grouped according to number of traditional risk factors and heart score was used to assess the risk of event for those with no CAC, those with only cMS > 0 and those with both AS and cMS > 0.Results: In participants with an AS = 0, 11% had cMS > 0. The risk profile of this cMS-only group was between that of the CAC-negative participants and those with AS > 0 and cMS > 0. Overall, 6% of the population belonged to the cMS-only group independent of the number of risk factors.Conclusion: In individuals with AS = 0, a fraction was found to have cMS > 0. Based on traditional risk factors, this group has a higher 10-year risk than individuals with both AS = 0 and cMS = 0; cMS might offer very early cardiovascular risk assessment in asymptomatic individuals.Key Points: • In individuals with AS=0, a fraction has CAC with highly sensitive cMS. • This fraction has a higher 10-year risk of cardiovascular disease. • Regardless of risk factors, 6% has CAC detectable only with cMS. • cMS might offer very early cardiovascular risk assessment in asymptomatic individuals. [ABSTRACT FROM AUTHOR]

OBJECTIVES:We tested the hypothesis that alcohol, alone and in combination with alcohol dehydrogenase (ADH) 1B and ADH1C genotypes, affects liver damage and disease in the general population.METHODS:Information on alcohol intake and on liver disease was obtained from 9,080 men and women from the Copenhagen City Heart Study. Biochemical tests for the detection of liver damage were specific for alanine aminotransferase (ALT), aspartate aminotransferase (AST)-to-ALT ratio (AST/ALT), γ-glutamyl transpeptidase (γ-GT), albumin, bilirubin, alkaline phosphatase, coagulation factors, and erythrocyte volume.RESULTS:Increasing alcohol intake was associated with increasing erythrocyte volume, AST/ALT, and levels of ALT, γ-GT, albumin, bilirubin, coagulation factors, and with decreasing levels of alkaline phosphatase. Multifactorially adjusted hazard ratios for alcoholic liver disease overall were 0.9 (95% confidence interval (CI), 0.6–1.4), 1.4 (0.8–2.5), 1.8 (0.9–3.5), and 4.1 (2.5–7.0) for an alcohol intake of 1–13, 14–20, 21–27, and ≥28 drinks per week, respectively, compared with drinking <1 drink per week (P for trend<0.0001); the corresponding hazard ratios for alcoholic liver cirrhosis were 1.7 (0.6–4.7), 2.0 (0.8–7.1), 6.5 (2.0–21), and 13 (4.6–37) (P for trend<0.0001). ADH1B and ADH1C genotypes were not associated with and did not modify the effect of alcohol on biochemical tests or risk of liver disease.CONCLUSIONS:Increasing alcohol intake from none to low (1–6 drinks per week) through to moderate (7–20 drinks per week) and excessive intake (≥21 drinks per week) leads to stepwise increases in signs of liver damage with no threshold effect, and to an increased risk of liver disease. The minor changes in biochemical tests for low alcohol intake may not account for subclinical liver disease. [ABSTRACT FROM AUTHOR]